3 - DERMATOSES RESULTING FROM PHYSICAL FACTORS Flashcards
Discuss First degree burns
result merely in an active congestion of the superficial blood vessels, causing erythema that may be followed by epidermal desquamation (peeling). Ordinary sunburn is the most common example of a first-degree burn. The pain and increased surface heat may be severe, and some constitutional reaction can occur if the involved area is large.
Discuss second degree burns
- In the superficial second-degree burn, there is a transudation of serum from the capillaries, which causes edema of the superficial tissues. Vesicles and bullae are formed by the serum gathering beneath the outer layers of the epidermis. Comple e recovery without scarring is usual in patients with superficial burns.
- The deep second-degree burn is pale and anesthetic. Injury to the reticular dermis compromises blood flow and destroys appendages, so healing takes more than 1 month and results in scarring.
Discuss third degree burns
involve loss of the full thickness of the dermis and often some of the subcutaneous tissues. Because the skin appendages are destroyed, there is no epithelium available for regeneration of the skin. An ulcerating wound is produced, which on healing leaves a scar.
Discuss fourth degree burns
involve the destruction of the entire skin, including the subcutaneous fat, and any underlying tendons
How do you treat minor burns?
Immediate first aid for minor thermal burns consists of prompt cold applications (ice water, or cold tap water if no ice is available), which are continued until pain does not return on stopping them.
What will you do in the presence of vesicles and bullae of 2nd dregree burns/
The vesicles and bullae of second-degree burns should not be opened but should be protected from injury because they form a natural barrier against contamination by microorganisms. If they become tense and unduly painful, the fluid may be evacuated under strictly aseptic conditions by puncturing it with a sterile needle, allowing collapse onto the underlying wound.
When will you recommend referral to a burn center?
Give examples of dispersing agents that facilitate removal of hot tar from buns
Polyoxyethylene sorbitan in bacitracin zinc–neomycin–polymyxin B (e.g , Neosporin) ointment, vitamin E ointment, and sunflower oil are excellent dispersing agents that facilitate the removal of hot tar from burns.
Define Miliaria
retention of sweat as a result of occlusion of eccrine sweat ducts, produces an eruption that is common in hot, humid climates, such as in the tropics and during the hot summer months in temperate climates
What organism produces an extracellular polysaccharide substance, induces miliaria in an experimental setting?
S. Epidermdis
This polysaccharide substance may obstruct the delivery of sweat to the skin surface. The occlusion prevents normal secretion from the sweat glands, and eventually pressure causes rupture of the sweat gland or duct at different levels. The escape of sweat into the adjacent tissue produces miliaria. Depending on the level of the injury to the sweat gland or duct, several different forms are recognized.
Describe Miliaria Crystallina.
Miliaria crystallina is characterized by small, clear, superficial vesicles with no inflammatory reaction
It appears in bedridden patients whose fever produces increased perspiration or when clothing prevents dissipation of heat and moisture, as in bundled children. Hypernatremia without fever may induce it.
The lesions are generally asymptomatic, and their duration is short-lived because they tend to rupture at the slightest trauma. Drugs such as isotretinoin, adrenergic/cholinergic drugs, and doxorubicin may induce it. The lesions are self-limited; no treatment is required.
Describe miliaria rubra
The lesions of miliaria rubra appear as discrete, extremely pruritic, erythematous papulovesicles (Fig. 3.4) accompanied by a sensation of prickling, burning, or tingling.
They later may become confluent on a bed of erythema. The sites most frequently affected are the antecubital and popliteal fossae, trunk, inframammary areas (especially under pendulous breasts), abdomen (especially at the waistline), and inguinal regions; these sites frequently become macerated because evaporation of moisture has been impeded. Exercise-induced itching or that of atopic dermatitis may also be caused by miliaria rubra. The site of injury and sweat escape is in the prickle cell layer, where spongiosis is produced.
Descibe miliaria pustulosa
Miliaria pustulosa is preceded by another dermatitis that has produced injury, destruction, or blocking of the sweat duct. The pustules are distinct, superficial, and independent of the hair follicle. The pruritic pustules occur most frequently on the intertriginous areas, flexural surfaces of the extremities, scrotum, and back of bedridden patients. Contact dermatitis, lichen simplex chronicus, and intertrigo are some of the associated diseases, although pustular miliaria may occur several weeks after these diseases have subsided. Recurrent episodes may be a sign of type I pseudohypoaldosteronism, because salt-losing crises may precipitate miliaria pustulosa or rubra, with resolution after stabilization.
Describe miliaria profunda
Nonpruritic, flesh-colored, deep-seated, whitish papules characterize miliaria profunda. It is asymptomatic, usually lasts only 1 hour after overheating has ended, and is concentrated on the trunk and extremities. Except for the face, axillae, hands, and feet, where here may be compensatory hyperhidrosis, all the sweat glands are nonfunctional. The occlusion is in the upper dermis. Miliaria profunda is observed only in the tropics and usually follows a severe bout of miliaria rubra.
results from occlusion of sweat ducts and pores, and it may be severe enough to impair an individual’s ability to perform sustained work in a hot environment
Postmiliarial Hypohidrosis
Affected persons may show decreasing efficiency, irritability, anorexia, drowsiness, vertigo, and headache; they may wander in a daze.
It has been shown that hypohidrosis invariably follows miliaria, and that the duration and severity of the hypohidrosis are related to the severity of the miliaria. Sweating may be depressed to half the normal amount for as long as 3 weeks.
rare form of miliaria with longlasting poral occlusion, which produces anhidrosis and heat retention
Tropical Anhidrotic Asthenia
What is the treatment for miliaria?
The most effective treatment for miliaria is to place the patient in a cool environment.
Even a single night in an air-conditioned room helps to alleviate the discomfort. Circulating air fans can also be used to cool the skin. Anhydrous lanolin resolves the occlusion of pores and may help to restore normal sweat secretions. Hydrophilic ointment also helps to dissolve keratinous plugs and facilitates the normal flow of sweat. Soothing, cooling baths containing colloidal oatmeal or cornstarch are beneficial if used in moderation. Patients with mild cases may respond to dusting powders, such as cornstarch or baby talcum powder.
What is erythema ab igne?
persistent erythema—or the coarsely reticulated residual pigmentation resulting from it—that is usually produced by long exposure to excessive heat without the production of a burn.
t begins as a mottling caused by local hemostasis and becomes a reticulated erythema, leaving pigmentation. Multiple colors are simultaneously present in an active patch, varying from pale pink to old rose or dark purplish brown. After the cause is removed, the affection tends to disappear gradually, bu sometimes the pigmentation is permanent.
Histologically, an increased amount of elastic tissue in the dermis is noted. The changes in erythema ab igne are similar to those of actinic elastosis. Interface dermatitis and epithelial atypia may be noted.
Erythema ab igne on the legs results from habitually warming them in front of open fireplaces, space heaters, or car heaters. Similar changes may be produced on the lower back or at other sites of an electric heating pad application, on the upper thighs with laptop computers, or on the posterior thighs from heated car seats. The reason for chronically exposing the skin to heat may be pain from an underlying cancer, or from a condition which predisposes to a feeling of cold, such as anorexia nervosa. The condition occurs also in cooks, silversmiths, and others exposed over long periods to direct moderate heat.
Epithelial atypia, which may lead to Bowen disease and squamous cell carcinoma, has rarely been reported to occur overlying erythema
ab igne. In remote areas of Kashmir, Kangr fire pots can induce erythema ab igne and cancer within the affected area. Treatment with 5-fluorouracil (5-FU), imiquimod, or photodynamic therapy may be effective in reversing this epidermal alteration.
The use of emollients containing α-hydroxy acids or a cream containing fluocinolone acetonide 0.01%, hydroquinone 4%, and tretinoin 0.05% may help reduce the unsightly pigmentation, as may treatment with the Q-switched neodymium-doped yttriumaluminum-garnet (Nd:YAG) laser.
How does exposure to cold damage the skin?
• Reduced temperature directly damages the tissue, as in frostbite and cold immersion foot.
• Vasospasm of vessels perfusing the skin prevents adequate perfusion of the tissue and causes vascular injury and consequent tissue injury (pernio, acrocyanosis, and frostbite).
• In unusual circumstances, adipose tissue is predisposed to damage by cold temperatures because of fat composition or location
Outdoor workers and recreationalists, military service members, alcoholic persons, and homeless people are particularly likely to sustain cold injuries. Maneuvers to treat orthopedic injuries or heatstroke and cooling devices for other therapeutic use may result in cold injuries ranging from acrocyanosis to frostbite. Holding ice coated with salt (salt and ice challenge) will induce cold-induced blistering.
Refers to persistent blue discoloration of the entire hand or foot worsened by cold exposure
Acrocyanosis
The hands and feet may be hyperhidrotic (Fig. 3.6). It occurs chiefly in young women. Cyanosis increases as the temperature decreases and changes to erythema with elevation of the dependent part. The cause is unknown. Smoking should be avoided.
Acrocyanosis with swelling of the nose, ears, and dorsal hands may occur after inhalation of butyl nitrite. Interferon alpha-2a and beta may induce it. Repeated injection of the dorsal hand with narcotic drugs may produce lymphedema and an appearance similar to the edematous phase of scleroderma. This so-called puffy hand syndrome may include erythema or a bluish discoloration of the digits. Patients with anorexia nervosa frequently manifest acrocyanosis as well as perniosis, livedo reticularis, and acral coldness. It may improve with weight gain. Approximately one third of patients with skin findings of POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, M component, skin changes) have acrocyanosis. Also, in patients with a homozygous mutation in SAMDH1 and cerebrovascular occlusive disease, acrocyanosis was frequent.
Acral vascular syndromes, such as gangrene, Raynaud phenomenon, and acrocyanosis, may be a sign of malignancy. In 47% of 68 reported cases, the diagnosis of cancer coincided with the onset of the acral disease. If such changes appear or worsen in an elderly patient, especially a man, without exposure to vasoconstrictive drugs or prior autoimmune or vascular disorders, a paraneoplastic origin should be suspected.
How do you distinguish acrocyanosis from raynaud syndrome?
Acrocyanosis is distinguished from Raynaud syndrome by its persistent (rather than episodic) nature and lack of tissue damage (ulceration, distal fingertip resorption).
constitutes a localized erythema and swelling caused by exposure to cold
Pernio (Chilblains, Perniosis)
Blistering and ulcerations may develop in severe cases. In people predisposed by poor peripheral circulation, even moderate exposure to cold may produce chilblains. Cryoglobulins, cryofibrinogens, antiphospholipid antibodies, or cold agglutinins may be present and pathogenic. Chilblain-like lesions may occur in discoid and systemic lupus erythematosus (SLE; chilblain lupus), particularly the TREX1-associated familial type, as a presenting sign of leukemia cutis, or if occurring in infancy may herald the Nakajo-Nishimura syndrome or the Aicardi-Goutières and Singleton-Merten syndrome. The chronic use of crack cocaine and its attendant peripheral vasoconstriction will lead to perniosis with cold, numb hands and atrophy of the digital fat pads, especially of the thumbs and index fingers, as well as nail curvature.
Pernio occur chiefly on the feet, hands, ears, and face, chiefly in women; onset is enhanced by dampness (Fig. 3.7). In surgery technicians, the hands are affected if an orthopedic cold therapy system is used; the skin under the device develops the lesions. The lateral thighs are involved in women equestrians who ride
on cold, damp days and the hips in those wearing tight-fitting jeans with a low waistband. Wading across cold streams may produce similar lesions. Nondigital lesions of cold injury can be nodular.
Patients with chilblains are often unaware of the cold injury when it is occurring, but later burning, itching, and redness call it to their attention. The affected areas are bluish red, with the color partially or totally disappearing on pressure, and are cool to the touch. Sometimes the extremities are clammy because of excessive sweating. As long as the dampness and cold exposure continues, new lesions will continue to appear. Investigation into an underlying cause should be undertaken in patients with pernio that is recurrent, chronic, extending into warm seasons, or poorly responsive to treatment.
Pernio histologically demonstrates a lymphocytic vasculitis. There is dermal edema, and a superficial and deep perivascular, tightly cuffed, lymphocytic infiltrate. The infiltrate involves the vessel walls and is accompanied by characteristic “fluffy” edema of the vessel walls.
How do you treat pernio?
The affected parts should be protected against further exposure to cold or dampness. If the feet are involved, woolen socks should be worn at all times during the cold months. Because patients are often not conscious of the cold exposure that triggers the lesions, appropriate dress must be stressed, even if patients say they do not sense being cold. Because central cooling triggers peripheral vasoconstriction, keeping the whole body (not just the affected extremity) warm is critical. Heating pads may be used judiciously to warm the parts. Smoking is strongly discouraged.
Nifedipine, 20 mg three times a day, has been effective. Vasodilators such as nicotinamide, 500 mg three times a day, or dipyridamole, 25 mg three times a day, or the phosphodiesterase inhibitor sildenafil, 50 mg twice daily, may be used to improve circulation. Pentoxifylline and hydroxychloroquine may be effective. Spontaneous resolution occurs without treatment in 1–3 weeks. Systemic corticoid therapy is useful in chilblain lupus.
When soft tissue is frozen and locally deprived of blood supply, the damage is called
Frostbite
The ears, nose, cheeks, fingers, and toes are most often affected. The frozen part painlessly becomes pale and waxy. Various degrees of tissue destruction similar to that caused by burns are encountered. These are erythema and edema, vesicles and bullae, superficial gangrene, deep gangrene, and injury to muscles, tendons, periosteum, and nerves (Fig. 3.8). The degree of injury is directly related to the temperature and duration of freezing. African Americans are at increased risk of fros bite. Arthritis of the small joints of the hands and feet may appear months to years later.
Treatmen of frostbite
Early treatment of frostbite before swelling develops should consist of covering the part with clothing or with a warm hand or other body surface to maintain a slightly warm temperature so that adequate blood circulation can be maintained. Rapid rewarming in a water bath between 37°C and 43°C (100°F and 110°F) is the treatment of choice for all forms of frostbite. Rewarming should be delayed until the patient has been removed to an area where there is no risk of refreezing. Slow thawing results in more extensive tissue damage Analgesics should be administered because of the considerable pain experienced with rapid thawing When the skin flushes and is pliable, thawing is complete The use of tissue plasminogen activator to lyse thrombi decreases the need for amputation if given within 24 hours of injury. Infusion of the vasodilator iloprost may be used if available. Supportive measures such as bed rest, a high-protein/high-calorie diet, wound care, and avoidance of trauma are imperative. Any rubbing of the affected part should be avoided, but gentle massage of proximal portions of the extremity that are not numb may be helpful.
The use of anticoagulants to prevent thrombosis and gangrene during the recovery period has been advocated. Pentoxifylline, ibuprofen, and aspirin may be useful adjuncts. Antibiotics should be given as a prophylactic measure against infection, and tetanus immunization should be updated. Recovery may take many months. Injuries that affect the proximal phalanx or the carpal or tarsal area, especially when accompanied by a lack of radiotracer uptake on bone scan, have a high likelihood of requiring amputation. Whereas prior cold injury is a major risk factor for recurrent disease, sympathectomy may be preventive against repeated episodes. Arthritis may be a late complication.
results from prolonged exposure to cold, wet conditions without immersion or actual freezing
Trench foot
The term is derived from trench warfare in World War I, when soldiers stood, sometimes for hours, in trenches with a few inches of cold water in them. Fishermen, sailors, and shipwreck survivors may be seen with this condition. The lack of circulation produces edema, paresthesias, and damage to the blood vessels. Similar findings may complicate the overuse of ice, cold water, and fans by patients trying to relieve the pain associated with erythromelalgia. Gangrene may occur in severe cases. Treatment consists of removal from the causal environment, bed rest, and restoration of the circulation. Other measures, such as those used in the treatment of frostbite, should be employed.
Exposure of the feet to warm, wet conditions for 48 hours or more may produce a syndrome characterized by
maceration, blanching, and wrinkling of the soles and sides of the feet
Itching and burning with swelling may persist for a few days after removal of the cause, but disability is temporary. This condition was often seen in military service members in Vietnam but has also been seen in persons wearing insulated boots.
Warm water immersion foot can be prevented by allowing the feet to dry for a few hours in every 24 or by greasing the soles with a silicone grease once a day. Recovery is usually rapid if the feet are thoroughly dry for a few hours.
*I think the picture pertains to warm water immersion foot
Warm water immersion foot should be differentiated from tropical immersion foot, seen after continuous immersion of the feet in water or mud at temperatures above 22°C (71.6°F) for 2–10 days. This was known as “paddy foot” in Vietnam. It involves erythema, edema, and pain of the dorsal feet, as well as fever and adenopathy (Fig. 3 10). Resolution occurs 3–7 days after the feet have been dried
The parts of the solar spectrum important in p medicine include UV radiation (______ nm), visible light (_____ nm), and infrared radiation (beyond ____ nm).
The parts of the solar spectrum important in p medicine include UV radiation (below 400 nm), visible light (400–760 nm), and infrared radiation (beyond 760 nm).
Visible light has limited biologic activity, except for stimulating the retina. Infrared radiation is experienced as radiant heat. Below 400 nm is the UV spectrum, divided into three bands:
- UVA, 320 400 nm;
- UVA is divided into two subcategories:
- UVA I (340–400 nm) and
- UVA II (320–340 nm)
- UVA is divided into two subcategories:
- UVB, 280–320 nm; and
- UVC, 200–280 nm.
- Virtually no UVC reaches the Earth’s surface because it is absorbed by the ozone layer above the Earth.
The minimal amount of a particular wavelength of light capable of inducing erythema on an individual’s skin is called the
Minimal Erythema Dose (MED)
Although he amount of UVA radiation is 100 times greater than UVB radiation during midday hours, UVB is up to 1000 times more erythemogenic than UVA, and so essentially all solar erythema is caused by UVB.
The most biologically effective wavelength of radiation from the sun for sunburn is ______
308 nm
Although it does not play a significant role in solar erythema, UVA is of major importance in patients with druginduced photosensitivity and also play a role in photoaging and cutaneous immunosuppression.
The amount of UV exposure increases at higher altitudes, is substantially larger in temperate climates in the summer months, and is greater in tropical regions. UVA may be reflected somewhat more than UVB from sand, snow, and ice. Whereas sand and snow reflect as much as 85% of the UVB, water allows 80% of the UV o penetrate up to 3 feet. Cloud cover, although blocking substantial amounts of visible light, is a poor UV absorber. During the middle 4–6 hours of the day, the intensity of UVB is 2–4 times greater than in the early morning and late afternoon
When does UVB erythema becomes evident?
At around 6 hours after exposure and peaks at 12–24 hours, but the onset is sooner and the severity greater with increased exposure.
The erythema is followed by tenderness and in severe cases, blistering, which may become confluent (Fig. 3.11). Discomfort may be severe; edema typically occurs in the extremities and face; chills, fever, nausea, tachycardia, and hypotension may be present. In severe cases, such symptoms may last for as long as a week. Desquamation is common about 1 week after sunburn, even in areas that have not blistered.
F g. 3.11 Acute sunburn
It is the normal cutaneous reaction to sunlight in excess of an erythema dose.
Sunburn
What changes does the skin pigent undergo after UV exposure?
immediate pigment darkening (IPD, Meirowsky phenomenon) and delayed melanogenesis
IPD is maximal within hours after sun exposure and results from metabolic changes and redistribution of the melanin already in the skin. It occurs after exposure to long-wave UVB, UVA, and visible light. With large doses of UVA, the initial darkening is prolonged and may blend into the delayed melanogenesis. IPD is not photoprotective. Delayed tanning is induced by the same wavelengths of UVB that induce erythema, begins 2–3 days after exposure, and lasts 10–14 days. Delayed melanogenesis by UVB is mediated through the production of DNA damage and the formation of cyclobutane pyrimidine dimers (CPD). Therefore, although UVB-induced delayed tanning does provide some protection from further solar injury, it is at the expense of damage to the epidermis and dermis. Tanning is not recommended for sun protection. Commercial tanning bed–induced tanning, while increasing skin pigment, does not increase UVB MED and is therefore not protective for UVB damage. Such tanning devices have been shown to cause melanoma, and their use for tanning purposes should be banned. An individual’s inherent baseline pigmentation, ability to tan, and susceptibility to burns are described as the person’s “skin type.” Skin type is used to determine starting doses of phototherapy and sunscreen recommendations and reflects the risk of development of skin cancer and photoaging (Table 3 1).
Exposure to UVB and UVA causes an increase in the thickness of
epidermis, especially the stratum corneum
This increased epidermal thickness leads to increased tolerance to further solar radiation. Patients with vitiligo may increase their UV exposure without burning by this mechanism.
Discuss treatment for sunburn
Once redness and other symptoms are present, treatment of sunburn has limited efficacy. The damage is done, and the inflammatory cascades are triggered. Prostaglandins, especially of the E series, are important mediators. Aspirin (acetylsalicylic acid [ASA]) and nonsteroidal antiinflammatory drugs (NSAIDs), including indomethacin, have been studied, as well as opical and systemic steroids. Medium-potency (class II) topical steroids applied 6 hours after the exposure (when erythema first appears) provide a small reduction in signs and symptoms. Oral NSAIDs and systemic steroids have been tested primarily before or immediately after sun exposure, so there is insufficient evidence to recommend their routine use, except immediately after solar overexposure. Therefore treatment of sunburn should be supportive, with pain management (using acetaminophen, ASA, or NSAIDs), plus soothing topical emollients or corticosteroid lotions. In general, a sunburn victim experiences at least 1 or 2 days of discomfort and even pain before much relief occurs.
Prophylaxis for sunburn
Use of the UV index facilitates taking adequate precautions to prevent solar injury. Numerous educational programs have been developed to make the public aware of the hazards of sun exposure. Despite this, sunburn and excessive sun exposure continue to occur in the United States and Western Europe, especially in white persons under age 30, more than 50% of whom report at least one sunburn per year. Sun protection programs have the following four main messages:
• Avoid midday sun.
• Seek shade.
• Wear sun-protective clothing.
• Apply a sunscreen.
When is the period of highest UVB intensity?
between 9 AM and 3–4 PM, accounts for the vast majority of potentially hazardous UV exposure.
This is the time when the angle of the sun is less than 45 degrees, or when a person’s shadow is shorter than his or her height. In temperate latitudes, it is almost impossible to burn if these hours of sun exposure are avoided. Trees and artificial shade provide substantial protection from UVB. Foliage in trees provides the equivalent of sun protection factor (SPF) 4–50, depending on the density of the greenery. Clothing can be rated by its ability to block UVB radiation.
The scale of measure is the UV protection factor (UPF), analogous to SPF in sunscreens. Although it is an in vitro measurement, UPF correlates well with the actual protection the product provides in vivo. In general, denser weaves, washed older clothing, and loose-fitting clothes screen UVB more effectively. Wetting a fabric may substantially reduce its UPF. Laundering a fabric in a Tinosorb-containing material (SunGuard) will add substantially to the UPF of the fabric. Hats with at least a 4-inch brim all around are recommended.
A sunscreen’s efficacy in blocking the UVB (sunburn-inducing) radiation is expressed as an _______
sun protection factor (SPF)
This is the ratio of the number of MEDs of radiation required to induce erythema through a film of sunscreen (2 mg/cm2 ) compared with unprotected skin. Most persons apply sunscreens in too thin a film, so the actual “applied SPF” is about half that on the label. Sunscreen agents include UV absorbing chemicals (chemical sunscreens) and UV-sca tering or blocking agents (physical sunscreens). Available sunscreens, especially those of high SPFs (>30), usually contain both chemical sunscreens (e.g , p-aminobenzoic acid [PABA], PABA esters, cinnamates, salicylates, anthranilates, benzophenones, benzylidene camphors such as ecamsule [Mexoryl], dibenzoylmethanes [Parsol 1789, in some products present as multicompound technology Helioplex], and Tinosorb [S/M]) and physical agents (zinc oxide or titanium dioxide). Sunscreens are available in numerous formulations, including sprays, gels, emollient creams, and wax sticks. Sunscreens may be water resistant, with some maintaining their SPF after 40 minutes of water immer sion and others maintaining their SPF after 80 minutes of water immersion.
For skin types I to III, what is the recomended sunscreen?
For skin types I to III (see Table 3.1), daily application of a broad-spectrum sunscreen with an SPF of 30 in a facial moisturizer, foundat on, or aftershave is recommended.
For outdoor exposure, a sunscreen of SPF 30 or higher is recommended for regular use. In persons with severe photosensitivity and at times of high sun exposure, high-intensity sunscreens of SPF 30+ with inorganic blocking agents may be required. Application of the sunscreen at least 20 minutes before and 30 minutes after sun exposure has begun is recommended. This dual-application approach will reduce the amount of skin exposure by twofold to threefold over a single application. Sunscreen should be reapplied after swimming or vigorous activity or toweling. Sunscreen failure occurs mostly in men, from failure to apply it to all the sun-exposed skin or failure to reapply sunscreen after swimming. Sunscreens may be applied to babies (under 6 months) on limited areas. Vitamin D supplementation is recommended with the most stringent sun protection practices. The dose is 600 IU daily for those 70 and younger and 800 IU for older patients.
Photoaging and cutaneous immunosuppression are mediated by
UVA as well as UVB
For this reason, sunscreens with improved UVA coverage have been developed. Those containing excellent protection for both UVB and UVA are identified on the label by the words “broad spectrum,” and these sunscreens should be sought by patients.
small (<0.5 cm) brown macules that occur in profusion on the sun-exposed skin of the face, neck, shoulders, and backs of the hands
Ephelis (Freckle)
They become prominent during the summer when exposed to sunlight and subside, sometimes completely, during the winter when there is no exposure. Blonds and redheads with blue eyes and of Celtic origin (skin types I or II) are especially susceptible. Ephelides may be genetically determined and may recur in successive generations in similar locations and patterns. They usually appear at about age 5 years.
benign, discrete hyperpigmented macule appearing at any age and on any part of the body, including the mucosa
Lentigo
The intensity of the color is not dependent on sun exposure. The solar lentigo appears at a later age, mostly in persons with long-term sun exposure The backs of the hands and face (especially the forehead) are favored sites (Fig. 3.12).
Fig. 3.12 Solar lentigines.
Histologically, the ephelis shows increased production of melanin pigment by a normal number of melanocytes. Otherwise, the epidermis is normal, whereas the lentigo has elongated rete ridges that appear to be club shaped.
How are freckles and solar lentigines prevented?
Freckles and solar lentigines are best prevented by appropriate sun protection. Cryotherapy, topical retinoids, hydroquinone, intense pulse light, undecylenoyl phenylalanine, and lasers are effective in the treatment of solar lentigines.
The characteristic changes induced by chronic sun exposure are called
photoaging or dermatoheliosis
An individual’s risk for developing these changes correlates with the person’s skin type (see Table 3.1). Risk for melanoma and nonmelanoma skin cancer is also related to skin type.
The persons most susceptible to the deleterious effects of sunlight are those of what skin type?
skin type I: blue-eyed, fair-complexioned persons who do not tan
They are frequently of Irish or other Celtic or Anglo-Saxon descent. Individuals who develop photoaging have the genetic susceptibility and have had sufficient actinic damage to develop skin cancer, and they therefore require more frequent and careful cutaneous examinations.
Chronic sun exposure and chronologic aging are additive. Cigarette smoking is also important in the development of wrinkles, resulting in the inability of observers to distinguish solar-induced from smoking-induced skin aging accurately. The areas primarily affected by photoaging are those regularly exposed to the sun: the V area of the neck and chest, back and sides of the neck, face, backs of the hands and extensor arms, and in women the skin between the knees and ankles. The skin becomes atrophic, scaly, wrinkled, inelastic, or leathery with a yellow hue (milian citrine skin). In some persons of Celtic ancestry, dermatoheliosis produces profound epidermal atrophy without wrinkling, resulting in an almost translucent appearance of the skin through which hyperplastic sebaceous glands and prominent telangiectasias are seen (Fig. 3.13). These persons are at high risk for nonmelanoma skin cancer. Pigmentation is uneven, with a mixture of poorly demar cated, hyperpigmented and white atrophic macules observed. The photodamaged skin appears generally darker because of these irregularities of pigmentation; in addition, dermal hemosiderosis occurs from actinic purpura. Solar lentigines occur on the face and dorsa of the hands.
Fig. 3.13 Dermatoheliosis.
refers to reticulate hyperpigmentation with telangiectasia, and slight atrophy of the sides of the neck, lower anterior neck, and V of the chest. The submental area, shaded by the chin, is spared (Fig. 3.14).
Fig. 3.14 Poikiloderma of Civatte
Poikiloderma of Civatte frequently presents in fair-skinned men and women in their mid to late thirties or early forties.
This is characteristic of long-term, chronic sun exposure (Fig. 3.15)
Fig. 3.15 Cutis rhomboidalis nuchae (sailor’s or farmer’s neck)
The skin on the back of the neck becomes thickened, tough, and leathery, and the normal skin markings are exaggerated.
. Nodular elastoidosis with cysts and comedones occurs on the inferior periorbital and malar skin on the forearms (actinic comedonal plaque) or helix of the ear.
Fig. 3.16 Favre-Racouchot Syndrome
These lesions appear as thickened yellow plaques studded with comedones and keratinous cysts. The ears may exhibit one or more firm nodules on the helix, known as weathering nodules. Biopsy reveals fibrosis and cartilage metaplasia.
nonimmunologic reaction that develops after exposure to a specific wavelength and intensity of light in the presence of a photosensitizing substance
phototoxic reaction
It is a sunburn-type reaction, with erythema, tenderness, and even blistering occurring only on the sun-exposed parts. This type of reaction can be elicited in many persons who have no previous history of exposure or sensitivity to that particular substance, but individual susceptibility varies widely. In general, to elicit a phototoxic reaction, a considerably greater amount of the photosensitizing substance is necessary than that needed to induce a photoallergic reaction. The erythema begins, as with any sunburn, within 2–6 hours but worsens for 48–96 hours before beginning to subside. Exposure of the nail bed may lead to onycholysis, called photo-onycholysis (Fig. 3.17). Phototoxic reactions, especially from topically applied photosensitizers, may cause marked hyperpigmentation, even without significant preceding erythema.
Fig. 3.17 Photo-onycholysis from minocycline.
Fig. 3.19 Severe phytophototoxicity
Most phototoxic plants are in the Umbelliferae, Rutaceae (rue), Compositae, and Moraceae families. Incriminated plants include agrimony, angelica, atrillal, bavachi, buttercup, common rice, cowslip, dill, fennel, fig, garden and wild carrot, garden and wild parsnip, gas plant, goose foot, zabon, lime and Persian lime (Fig. 3.18), lime bergamot, masterwort, mustard, parsley, St. John’s wort, and yarrow. In Hawaii, the anise-scented mokihana berry (Pelea anisata) was known to natives for its phototoxic properties (mokihana burn). It is a member of the rue family. Exposure through limes used to flavor gin and tonics and Mexican beer may result in phototoxic reactions in outdoor bartenders and their customers. Home tanning solutions containing fig leaves can produce phytophotoderma itis. These conditions may be widespread and severe enough to require burn unit management (Fig. 3.19).
Fig. 3.18 Two friends who made limeade in the sun to sell in the summer.
Occupa ional disability from exposure to the pink rot fungus (Sclerotinia sclerotiorum), present on celery roots, occurs in celery farmers. In addition, disease-resistant celery contains furocoumarins and may produce phytophotodermatitis in grocery workers. Usually, insufficient sensitizing furocoumarin is absorbed from dietary exposure; however, ingested herbal remedies may cause systemic phototoxicity.
phytophotodermatitis caused by contact not with grass, but with yellow-flowered meadow parsnip or a wild, yellow-flowered herb of the rose family
Dermatitis bullosa striata pratensis (grass or meadow dermatitis)
The eruption consists of streaks and bizarre configurations with vesicles and bullae that heal with residual hyperpigmentation. The usual cause is sunbathing in fields containing the phototoxic plants. Similarly, tourists in the tropics may rinse their hair with lime juice outdoors, and streaky hyperpigmentation of the arms and back will result where the lime juice runs down (Fig. 3.20).
Blistering phytophotodermatitis must be differentiated from rhus dermatitis. The vesicles and bullae of rhus are not necessarily limited to the sun-exposed areas, and itching is the most prominent symptom. Lesions continue to occur in rhus dermatitis for a week or more. In phytophotodermatitis, the reaction is limited to sunexposed sites, a burning pain appears within 48 hours, and marked hyperpigmentation results. The asymmetry, atypical shapes, and streaking of the lesions are helpful in establishing the diagnosis. These features may lead to a misdiagnosis of child abuse.
Treatment of a severe, acute reaction is similar to the management of a sunburn, with cool compresses, mild analgesics if required, and topical emollients. Use of topical steroids and strict sun avoidance immediately after the injury may protect against the hyperpigmentation. The hyperpigmentation is best managed by “tincture of time.”
Clinically, the eruption may have several different morphologies, although in the individual patient, the morphology is usually constant. What is the most common variant of Polymorphous Light Eruption?
The papular (or erythematopapular) variant is the most common, but papulovesicular, eczematous, erythematous, and plaquelike lesions also occur (Fig. 3.21).
Fig. 3.21 Polymorphous light eruption, papular type.
Plaquelike lesions are more common in elderly patients and may closely simulate lupus erythematosus, with indurated, erythematous, fixed lesions In African Americans, a pinpoint papular variant has been observed, closely simulating lichen nitidus but showing spongiotic dermatitis histologically (Fig. 3.22). Scarring and atrophy do not occur; in darkly pigmented races, however, marked postinflammatory hyperpigmentation or hypopigmentation may be present. In some patients, pruritus only, without an eruption, may be reported (PLE sine eruptione). Some of these patients will develop typical PLE later in life.
Fig. 3.22 Polymorphous light eruption, micropapular variant resembling lichen nitidus.
The lesions of PLE appear most often 1–4 days after exposure to sunlight, although patients may report itching and erythema during sun exposure and development of lesions within the first 24 hours. A change in the amount of sun exposure appears to be more critical than the absolute amount of radiation. Patients living in tropical climates may be free of eruption, only to develop disease when they move to temperate zones, where there is more marked seasonal variation in UV intensity. Areas of involvement include the face, the V area of the chest, neck, and arms. In general, for each individual, certain areas are predisposed. Typically, however, areas protected during the winter, such as the extensor forearms, are particularly affected, whereas areas exposed all year (face and dorsa of hands) may be relatively spared. The eruption appears most frequently in the spring. The eruption often improves with continued sun exposure (hardening), so patients may be clear of the condition in the summer or autumn.
Fig. 3.23 Juvenile spring eruption of the ears.
An unusual variant of PLE is juvenile spring eruption of the ears (Fig. 3.23). This occurs most frequently in boys age 5–12 years but may also be found in young adult males. It presents in the spring, often after sun exposure on cold but sunny days. The
typical lesions are grouped small papules or papulovesicles on the helices. Le ions may form visible vesicles and cru ting. Juvenile spring eruption of the ears is self-limited and does not scar. UVA is the inducing spectrum, and some patients also have lesions of PLE elsewhere. The histologic picture is identical to that of PLE. Another localized variant of PLE is spring and summer eruption of the elbows, but this occurs in adults, equally in men and women.
Histologically, a perivascular, predominantly T-cell infiltrate is present in the upper and middle dermis. There is often edema and endothelial swelling, with occasional neutrophils. Epidermal changes are variable, with spongiosis and exocytosis most often observed. Occasionally, a virtual absence of findings microscopically may paradoxically be reported and has been referred to as pauci inflammatory photodermatitis.
The reported action spectrum of PLE varies, possibly depending on the different ethnic backgrounds of reported populations. UVA is most often responsible; however, UVB and both wavelengths in combination are also frequently necessary. Patients often report eruptions following sun exposure through window glass. Although rare, visible light sensitivity can also occur. Typically, women are more sensitive than men to UVA only, and men are more sensitive to visible light. Men, although the minority of PLE patients, tend to have more severe PLE and broader wavelengths of sensitivity. Most patients react more in affected sites, and in some, lesions can only be induced in affected areas. Phototesting produces variable results. One protocol produced positive results in 83% of tested patients using four exposures of UVB, UVA, or a combination in previously affected sites. However, the light sources are not readily available, and reported protocols vary widely. In clinical practice, the diagnosis s usually made clinically.
Fig. 3.24 Actinic prurigo, prurigo nodularis–like lesions.
Actinic prurigo probably represents a variant of PLE; it is most often seen in Native Americans of North and Central America and Colombia. The incidence in Mexico has been reported at between 1.5% and 3.5% It has been reported in Europe, Australia, and Japan as well. The female/male ratio is between 2 : 1 and 6 : 1. Actinic prurigo in Native Americans in the United States begins before age 10 in 45% of cases and before age 20 in 72%. Up to 75% of patients have a positive family history (hereditary PLE of Native Americans). In Europe, 80% of cases occur before age 10. In the Inuit Canadian population, onset is later and frequently in adulthood.
In childhood, lesions begin as small papules or papulovesicles that crust and become impetiginized. They are intensely pruritic and frequently excoriated. In children, the cheeks, distal nose, ears, and lower lip are typically involved. Cheilitis may be the initial and only feature for years. Conjunctivitis is seen in 10%–20% of patients (limbal-type vernal catarrh). Lesions of the arms and legs are also common and usually exhibit a prurigo nodule–like configuration (Fig. 3.24). The eruption may extend to involve
sun-protected areas especially the buttocks, but lesions in these areas are always less severe. In adults, chronic, dry papules and plaques are most typical, and cheilitis and crusting occur less frequently. Skin lesions tend to persist throughout the year in the tropics but are clearly worse during periods of increased sun exposure. In temperate and high-latitude regions, lesions occur from March through the summer and substantially remit in the winter. Hardening, as seen with PLE, does not occur. In up to 60% of patients with actinic prurigo that present before age 20, the condition improves or resolves within 5 years, whereas adults usually have the disease throughout life.
Initial therapy is identical to that for PLE. Thalidomide has been used effectively and safely over many years for this condition. In patients refractory to or intolerant of thalidomide, cyclosporine can be effective. Topical cyclosporine 2% may be effective in controlling limbal lesions of actinic prurigo–associated conjunctivitis.
Fig. 3.25 Polymorphous light eruption, brachioradial distribution.
PLE may present initially and only on the brachioradial area. This type of brachioradial eruption was the initial pattern of brachioradial pruritus described and was termed solar pruritus (Fig. 3.25). The majority of cases of brachioradial pruritus, especially those characterized by severe, refractory, intractable pruritus and secondary severe lichenification, are now thought to represent a form of neuropathic pruritus, sometimes related to cervical spine disease (see Chapter 4). Sunlight may be an eliciting factor and cervical spine disease a predisposing factor in patients with brachioradial pruritus. To identify those patients in whom photosensitivity plays a prominent role, a high-SPF (UVA/UVB) sunscreen should be applied to one arm only for several weeks. In patients with PLE, this usually leads to improvement of that one arm compared with the contralateral unprotected arm. In patients with primarily neuropathic disease, sunscreen application leads to minimal improvement. The capsaicin patch provides both itch relief and a physical barrier but is expensive.
Within seconds to minutes after light exposure, typical urticarial lesions appear and resolve in 1–2 hours, rarely lasting more than 24 hours (Fig. 3.26).
Fig 3 26 Solar urticaria.
Solar urticaria is most common in women age 20–40. Delayed reactions rarely occur. Chronically exposed sites may have some reduced sensitivity. In severe attacks, syncope, bronchospasm, and anaphylaxis may occur.
Patients with solar urticaria may be sensitive to wavelengths over a broad spectrum. The wavelengths of sensitivity and the minimal urticarial doses (MUDs) may vary with anatomical site and over time within the same patient. UVA sensitivity is the most common, but visible light sensitivity is also frequently reported. The photosensitivity can be passively transferred, and irradiation of the patient’s serum with the activating wavelength followed by reinjection will create a wheal in the patient, but not in an unaffected patient. This suggests the presence of a circulating photoinducible allergen to which the individual patient with solar urticaria is sensitive. In some patients, an inhibition spectrum may be identified that inhibits the binding of the endogenous photoallergen to mast cells.
Solar urticaria is virtually always idiopathic. Rarely, medications such as tetracycline (but not minocycline), chlorpromazine, progestational agents, and repirinast have been reported to induce solar urticaria. Erythropoietic protoporphyria and more rarely porphyria cutanea tarda may present with lesions simulating solar
urticaria. There are rare reports of solar urticaria in patients with lupus erythematosus.
The diagnosis of solar urticaria is usually straigh forward from the history. Phototesting is useful to determine the wavelengths of sensitivity and to ascertain the MUD if UVA desensitization is being considered.
Because many patients have sensitivity in the UVA or even visible range, broad-spectrum sunscreens should be instituted. Antihistamines, especially the nonsedating H1 agents loratadine, cetirizine HCl, and fexofenadine, may increase the MUD 10-fold or more. Higher doses, twice or more the standard recommendation, may be required. These drugs, plus sun avoidance and broad-spectrum sunscreens, are the first-line therapy. The leukotriene receptor antagonist motelukast may provide additive efficacy when used in combination with the above regimen. PUVA or increasing UVA exposures are effective in more difficult cases, with PUVA having greater efficacy. Rush hardening may induce UVA tolerance, allowing patients to begin PUVA therapy. PUVA is effective, even if the patient is not sensitive to UVA. Cyclosporine (4.5 mg/kg/ day) and intravenous immune globulin at various doses and time frames have been anecdotally reported as effective. For the most difficult cases, plasmapheresis may be used to remove the circulating photoallergen, allowing PUVA to be given and leading to remission. Multiple reports attest to positive responses in some patients with the use of omalizumab.
What are the basic components of chronic actinic dermatitis?
• Persistent, chronic, eczematous eruption in the absence of exposure to known photosensitizers
• Usually, broad-spectrum photosensitivity with decreased MED to UVA and/or UVB and at times visible light
• Histology consistent with a chronic dermatitis, with or without features of lymphoma
Fig. 3.27 Chronic actinic dermatitis.
Clinically, chronic actinic dermatitis predominantly affects middle-age or elderly men. In the United States patients with skin types V and VI may be disproportionately affected (Fig. 3.27). Skin lesions consist of edematous, scaling, thickened patches and plaques that tend to be confluent. Lesions occur primarily or most severely on the exposed skin and may spare the upper eyelids, behind the ears, and the bottom of wrinkles. Involvement of unexposed sites often occurs, progressing to erythroderma in the most severe cases. Marked depigmentation resembling vitiligo
may result. Patients may not realize their condition is exacerbated by exposure to light. It may persist in all seasons.
The pathogenesis of this syndrome is unknown. In some patients, a preceding topical or oral photosensitizer may be implicated, but chronic actinic dermatitis fails to improve with discontinuation of the inciting agent. In about one third of patients, photopatch testing yields a positive response to previously applied agents, especially musk ambrette, sunscreen ingredients, p-phenylenediamine, and hexachlorophene. Patch testing to standard agents may have a positive result in about 30% of patients, but no particular relevance is found. However, in approximately 65% of European patients, sesquiterpene lactone contact sensitivity from Compositae has been identified. In addition, more than 75% of men over age 60 with sesquiterpene lactone sensitivity have abnormal phototesting results. CD8 (suppressor/cytotoxic) T cells are disproportionately represented in the cutaneous infiltrates in the majority of patients and less frequently in the peripheral blood. IgE levels may be elevated.
Acute Radiodermatitis
Fig. 3.28 Acute radiation burn during treatment of epithelioid sarcoma
When an “erythema dose” of ionizing radiation is given to the skin, there is a latent period of up to 24 hours before visible erythema appears. This initial erythema lasts 2–3 days but may be followed by a second phase beginning up to 1 week after the exposure and lasting up to 1 month. When the skin is exposed to a large amount of ionizing radiation, an acute reaction develops, the extent of which will depend on the amount, quality, genetic susceptibility, and duration of exposure. Such radiation reaction occurs in the treatment of malignancy and in accidental overexposure. The reaction is manifested by initial erythema, followed by a second phase of erythema at 3–6 days (Fig. 3.28). Vesiculation, edema, and erosion or ulceration may occur, accompanied by pain. The skin develops a dark color that may be mistaken for hyperpigmentation but that desquamates. This type of radiation injury may subside in several weeks to several months, again depending on the amount of radiation exposure. Skin that receives a large amount of radiation will never return to normal. It will lack adnexal structures, will be dry, atrophic, and smooth, and will be hypopigmented or depigmented. Cutaneous necrosis may complicate yttrium-90 synovectomy, a treatment given for chronic synovitis.
Fig. 3.29 (A) Fluoroscopy-induced radiodermatitis. (B) Close-up of Fig. 3.29A.
Chronic exposure to “suberythema” doses of ionizing radiation over a prolonged period will produce varying degrees of damage to the skin and its underlying parts after a variable latent period ranging from several months to several decades. Radiodermatitis may also occur on the back or flank after fluoroscopy and roentgenography for diagnostic or therapeutic purposes (Fig. 3.29).
Telangiectasia, atrophy, and hypopigmentation with residual focal increased pigment (freckling) may appear (Fig. 3.30). The skin becomes dry, thin, smooth, and shiny. The nails may become striated, brittle, and fragmented. The capacity to repair injury is substantially reduced, resulting in ulceration from minor trauma. The hair becomes brittle and sparse.
Fig 3.30 Chronic radiodermatitis.
Fig. 3.31 Delayed radiation reaction 8 months after therapy.
The hair becomes brittle and sparse. In more severe cases, these chronic changes may be followed by radiation keratoses and carcinoma. Additionally, subcutaneous fibrosis, thickening, and binding of the surface layers to deep tissues may present as tender, erythematous plaques 6–12 months after radiation therapy (Fig. 3.31). It may resemble erysipelas or inflammatory metastases.
Fig. 3.32 Chronic radiodermatitis w th basal cell cancer as a complication. (Courtesy Steven Binnick, MD.)
After a latent period averaging 20–40 years, various malignancies may develop, most frequently basal cell carcinoma (BCC), followed by squamous cell carcinoma (SCC). These may appear in sites of prior radiation, even if there is no evidence of chronic radiation damage. Sun damage may be additive to radiation therapy, increasing the appearance of nonmelanoma skin cancers. SCCs arising in sites of radiation therapy metastasize more frequently than purely sun-induced SCCs. In some patients, either type of tumor may predominate. Location plays some role; SCCs are more common on the arms and hands, whereas BCCs are seen on the head and neck and lumbosacral area (Fig. 3.32). Other radiationinduced cancers include angiosarcoma, Kaposi sarcoma, malignant fibrous histiocytoma, sarcomas, and thyroid carcinoma. The incidence of malignant neoplasms increases with the passage of time.
nonpenetrating, circumscribed hyperkeratosis produced by pressure
Fig. 3.33 Tennis toe.
Callus
It occurs on parts of the body subject to intermittent pressure, particularly the palms and soles, and especially the bony prominences of the joints. Those engaged in various sports, certain occupations, or other repetitive activity develop callosities of distinctive size and location as stigmata. Examples are surfer’s nodules, boxer’s knuckle pads, jogger’s toe, rower’s rump, playstation thumb, milker’s callus, tennis toe (Fig. 3.33), jogger’s nipple, prayer callus, the yoga sign, neck callosities of violinists, pillar knocker’s knuckles, bowler’s hand, and Russell sign. The latter are calluses, small lacerations, or abrasions on the dorsum of the hand overlying the metacarpophalangeal and interphalangeal joints and are seen as a clue to the diagnosis of bulimia nervosa.
Fig. 3.34 Fire coral cuts.
A severe type of skin injury may occur from the cuts of coral skeletons (Fig. 3.34) The abrasions and cuts are painful, and local therapy may provide little or no relief. Healing may take months. As a rule, if secondary infection is guarded against, such cuts heal as well as any others. The possibility of Mycobacterium marinum infection must be considered in persistent lesions
This lesion is a cordlike structure encircling the coronal sulcus of the penis or running the length of the shaft and has been attributed to trauma during vigorous sexual play (Fig. 3 35).
Sclerosing Lymphangiitis
Fig. 3.35 Sclerosing lymphangitis of penis.
Most if not all cases result from a superficial thrombophlebitis and thus has been renamed Mondor disease of the penis. Some early reports favor a lymphatic origin of some cases; CD31 and D240 stains will allow differentiation of future cases. Treatment is not necessary; sclerosing lymphangiitis follows a benign, self-limiting course.
A sudden shower of minute, black, punctate macules occurs most often on the posterior edge of the plantar surface of one or both heels (Fig. 3.36), but sometimes distally on one or more toes.
Black heel
Synonyms for black heel include talon noir and calcaneal petechiae. Black heel is often seen in basketball, volleyball, tennis, or lacrosse players. Seeming confluence may lead to mimicry of melanoma. The bleeding is caused by shearing stress of sports activities. Paring with a No. 15 blade and performing a guaiac test will confirm the diagnosis. Treatment is unnecessary.
Free air occurring in the subcutaneous tissues
Subcutaneous Emphysema
It is detected by the presence of cutaneous crepitations. Gas-producing organisms, especially Clostridia, and leakage of free air from the lungs or gastrointestinal tract are the most common causes (Fig. 3.37). Samlaska et al. reviewed the wide variety of causes of subcutaneous emphysema, including penetrating and nonpenetrating injuries, iatrogenic causes occurring during various procedures in hospitalized patients, spontaneous pneumomediastinum such as may occur with a violent cough, childbirth, asthma, Boerhaave syndrome (esophageal rupture after vomiting or the Heimlich maneuver), intraabdominal causes such as inflammatory bowel disease, cancer, perirectal abscess, pancreatitis or cystitis, dental procedures when using air pressure instruments and high-speed drills, and factitial disease.
Fig. 3.37 Subcutaneous emphysema. (Courtesy Curt Samlaska, MD )
this rare cause of painful feet represents fat herniations through thin fascial layers of the weight-bearing parts of the heel (Fig. 3.38).
Painful Fat Herniation , also called painful piezogenic pedal papules
These d toceles become apparent when weight is placed on the heel and disappear as soon as the pressure is removed. These fat herniations are present in many people, but the majority experience no symptoms. However, extrusion of the fat tissue together with its blood vessels and nerves may initiate pain on prolonged standing. Avoidance of prolonged standing will relieve this pain. Other options include taping of the foot, use of compression stockings, or use of plastic heel cups or padded orthotic devices to restrict the herniations. Laing et al. found that 76% of 29 patients had pedal papules, and interestingly, by placing pressure on the wrists, found 86% to have piezogenic wrist papules
Fig. 3.38 Piezogenic papules. (Courtesy Paul Hong, MD.)
Subcutaneous injection (“skin popping”) can result in multiple, scattered ulcerations, which heal with discrete atrophic scars (Fig. 3.39).
Fig. 3.39 Ulceration secondary to “skin popping.”
Narcotic Dermopathy
Heroin (diacetylmorphine) is a narcotic prepared for injection by dissolving the heroin powder in boiling water and then injecting it. The favored route of administration is intravenous. This results in thrombosed, cordlike, thickened veins at the sites of injection.
In addition, amphetamines, cocaine, and other drugs may be injected. Subcutaneous injection may result in infections, complications of bacterial abscess and cellulitis, or sterile nodules, apparently acute foreign body reactions to the injected drug or the adulterants mixed with it. These lesions may ulcerate. Chronic persistent firm nodules, a combination of scar and foreign body reaction, may result. If cocaine is being injected, it may cause ulcers because of its direct vasospastic effect. Addicts will continue to inject heroin and cocaine into the chronic ulcer bed. Cocaine-associated vasculitis caused by levamisole is discussed in Chapter 35.
The cutaneous manifestations of injection of heroin and other drugs also include camptodactylia, edema of the eyelids, persistent nonpitting edema of the hands, urticaria, abscesses atrophic scars, and hyperpigmentation. Pentazocine abuse leads to a typical clinical picture of tense woody fibrosis, irregular punched-out ulcerations, and a rim of hyperpigmentation at injection sites. Extensive calcification may occur within the thickened sites.
Fig. 3.40 Red tattoo reaction. (Courtesy Curt Samlaska, MD.)
Tattoo-associated dermopathies may be reactive (allergic, lichenoid, granulomatous, or photosensitive) (Fig. 3.40) or infective (inoculation of syphilis, infectious hepatitis, tuberculosis, HIV, warts, molluscum, Hansen disease) or may induce a Koebner response in patients with active lichen planus or psoriasis. Discoid lupus erythematosus has been reported to occur in the redpigmen ed portion of tattoos. Tattoos over nevi may delay the diagnosis of melanoma. Occasionally, the tattoo marks may become keloidal. Severe allergic reactions to “temporary tattoos” (painting of pigments such as henna on surface of skin) occur when the allergen p-phenylenediamine is added to make the color more dramatic.
Red tattoos are the most common cause of delayed reactions, with the histologic findings typically showing a lichenoid process. Occasionally, a pseudolymphomatous reaction may occur in red tattoos. Dermatitis in areas of red (mercury), green (chromium), or blue (cobalt) have been described in patients who are patch test positive to these metals. Sarcoidal, foreign body, and allergic granulomatous reactions may also occur within tattoos; aluminum may induce such reactions.
Treatment of such reactions is with topical or intralesional steroids Excision is also satisfactory when the lesions are small enough and situated so that ellipsoid excisions are feasible. Reactions may also be successfully treated with Q-switched lasers, at times combined with ablative fractional resurfacing Generalized allergic reactions occasionally occur; prevention by treatment with oral steroids and antihistamines has been suggested. Tattoo darkening can occur, as well as no response to laser treatment. Caution must be used when treating flesh-colored and pink-red tattoos because they may darken after treatment, likely caused by the reduction of ferric oxide to ferrous oxide. White ink, composed mostly of titanium dioxide, is often used to brighten green, blue, yellow, and purple tattoos. Laser irradiation reduces titanium to a bluecolored pigment. Test areas are recommended when treating light-colored facial tattoos. CO 2 resurfacing lasers used conservatively are an alternative to the Q-switched lasers in such patients
Silicone Granuloma
Fig. 3.42 Silicone granuloma.
Liquid silicones, composed of long chains of dimethyl siloxy groups, are biologically inert. Silicones have been used for correcting wrinkles, reducing scars, and building up atrophic depressed areas of the skin. Many case reports detail granulomatous reactions to silicone, some with migration and reactive nodules at points distant from the injection site (Figs. 3.41 and 3.42). Acupuncture needles are coated with silicone, and granulomas may occur at the entry points. The incidence of the nodular swellings, which may be quite destructive and treatment resistant, remains unknown. It is clear that, if used off label, medical-grade silicone injected in small volume should be the rule, and it should not be injected into the penis or the glandular tissue of the breast.
For breast augmentation, silicone may be used as Silastic implants. If trauma causes rupture of the bag, subcutaneous fibrotic nodules often develop. Bioplastique consists of polymerized silicone particles dispersed in a gel carrier. When used for lip augmentation, nodules may develop. Histologically, these are foreign body granulomas.
Treatment of silicone granulomas is often not successful. Surgical removal may lead to fistulas, abscesses, and marked deformity. Both minocycline, 100 mg twice daily for several months, and imiquimod cream have been anecdotally useful.
Fig. 3.41 Silicone reaction.
Mercury Granuloma
Fig. 3.43 Mercury granuloma from thermometer.
Mercury may cause foreign body giant cell or sarcoidal-type granulomas (Fig. 3.43), pseudolymphoma, or membranous fat necrosis. It is usually identifiable as egg-shaped, extracellular, dark-gray to black, irregular globules. The gold lysis test is positive in tissues. Energy-dispersive radiographic spectroscopy may be done and will identify mercury by the characteristic emission spike. Such testing may be helpful in identifying any foreign substance suspected to have been implanted accidentally or intentionally by the patient. Systemic toxicity or embolus may develop from mercury and may result in death. Therefore excision is necessary and can be accomplished under x-ray guidance.
A papular eruption involving the axillae is sometimes seen as an allergic reaction in those shaving their armpits and using a deodorant containing zirconium (Fig. 3.44)
Fig. 3.44 Aluminum-zirconium granuloma secondary to antiperspirant use.
Zirconium Granuloma
Although zirconium was eliminated from aerosol-type deodorants in 1978, aluminumzirconium complex is present in some antiperspirants. Additionally, various poison ivy lotions contain zirconium compounds. The lesions are brownish red, dome-shaped, shiny papules. This is an acquired, delayed-type, allergic reaction resulting in a granuloma of the sarcoidal type. After many months, the lesions involute spontaneously.
Automobile crashes and other types of trauma may produce tattooing of dirt (silicon dioxide) into the skin, which induces __________
Silica Granuloma
Fig. 3.45 (A and B) Silica granuloma years after motorcycle crash.
These typically present as black or blue papules or macules arranged in a linear fashion. At times, the granulomatous reaction to silica may be delayed for many years, with the ensuing reaction being both chronic and disfiguring. The granulomas may be caused by amorphous or crystalline silicon dioxide (quartz), magnesium silicate (talcum), or complex polysilicates (asbestos). Talc granulomas of the skin and peritoneum may develop after surgery from the talcum powder used on surgical gloves. Silica granulomas have a statistical association with systemic sarcoidosis, and silica may act as a stimulus for granuloma formation in patients wi h latent sarcoidosis.
Removal of these granulomas is fraught with difficulties. The best method of care is immediate and complete removal to prevent these reactions. Excision and systemic steroids have been used, but recurrences are common. Some reactions may subside spontaneously after 1–12 months. Dermabrasion or simple abrasion with a hard-bristled toothbrush is a satisfactory method for the removal of dirt accidentally embedded into the skin of the face or scalp.
Discoloration of the skin from embedded carbon usually occurs in children from improper use of firearms (Fig. 3.46) or fireworks or from a puncture wound by a pencil, which may leave a permanent black mark of embedded graphite, easily mistaken for a metastatic melanoma.
Fig. 3.46 Carbon stain, gunshot wound.
Narcotic addicts who attempt to clean needles by flaming them with a lighted match may tattoo the carbon formed on the needle as it is inserted into the skin.
Carbon particles may be removed immediately after their deposition using a toothbrush and forceps. This expeditious and meticulous early care results in the best possible cosmetic result. If the particles are left in place long enough, they are best removed using the Q-switched Nd:YAG laser at 1064 nm. In one series success was reported in 50 of 51 treated tattoos with an average of 1.7 treatments. However, microexplosions producing poxlike scars have occurred with each laser pulse. Alternatively, dermabrasion may be used.
Injected or implanted filler substances used for facial rejuvenation may produce foreign body or sarcoidal granulomas. Palpable thickening and nodules (Fig. 3.47), which are occasionally painful, have been reported with collagen, hyaluronic acid and acrylic hydrogels, and polylactic acid, polyalkylimide, and polymethylmethacrylate microspheres.
Fig. 3.47 Injected filler reaction.
The reaction may be delayed for years; at times, patients are reluctant to admit to these prior cosmetic interventions and frequently cannot name the filler used. Topical, intralesional, or systemic steroids, sometimes augmented by tacrolimus, and minocycline or doxycycline have been reported to be helpful medical interventions.
